LACK OF C-JUN EXPRESSION IN A TRANSFORMED-CELL LINE ISOLATED BY GLUCOCORTICOID PROMOTION OF RAS-TRANSFECTED RAT EMBRYO FIBROBLASTS

Rat embryo fibroblasts (REFs) are inefficiently transformed by the T24 -ras oncogene. A contributing factor to cellular resistance to transfo rmation is the limited tolerance to p21-ras oncoprotein expression. He re we present data suggesting that long-term glucocorticoid treatment of ras oncogene-transfected REFs results in increased tolerance to p21 -ras oncoproteins, leading to expression of the transformed phenotype. Stably transformed cell lines that expressed high levels of H-ras and could be maintained in the absence of hormone were isolated. In three out of four tines studied, the AP-1-dependent collagenase gene was ex pressed at a low level. In one of these lines, low collagenase express ion was paralleled by lack of c-jun mRNA. Immunochemical analysis reve aled that progression to hormone independence was not paralleled by mu tations in the p53 gene. We propose that a decreased expression of AP- 1-driven genes may result in increased tolerance to p21-ras oncoprotei n.